Taking the Scenic Route: Polyomaviruses Utilize Multiple Pathways to Reach the Same Destination

Abstract

Members of the Polyomaviridae family differ in their host range, pathogenesis, and disease severity. To date, some of the most studied polyomaviruses include human JC, BK, and Merkel cell polyomavirus and non-human subspecies murine and simian virus 40 (SV40) polyomavirus. Although dichotomies in host range and pathogenesis exist, overlapping features of the infectious cycle illuminate the similarities within this virus family. Of particular interest to human health, JC, BK, and Merkel cell polyomavirus have all been linked to critical, often fatal, illnesses, emphasizing the importance of understanding the underlying viral infections that result in the onset of these diseases. As there are significant overlaps in the capacity of polyomaviruses to cause disease in their respective hosts, recent advancements in characterizing the infectious life cycle of non-human murine and SV40 polyomaviruses are key to understanding diseases caused by their human counterparts. This review focuses on the molecular mechanisms by which different polyomaviruses hijack cellular processes to attach to host cells, internalize, traffic within the cytoplasm, and disassemble within the endoplasmic reticulum (ER), prior to delivery to the nucleus for viral replication. Unraveling the fundamental processes that facilitate polyomavirus infection provides deeper insight into the conserved mechanisms of the infectious process shared within this virus family, while also highlighting critical unique viral features.

A latent pathogen infection classification system that would significantly increase healthcare safety

“…Adeno-associated virus, used in gene therapy applications, may or may not help other pathogen infections during its latent infections; its effects will probably become more clearly understood in the near future [ 16 ]. Polyomavirus BK latently infects the renal urinary tract of most healthy individuals, and polyomavirus JC latently infects the kidneys of most healthy individuals, but they do not appear to help other pathogen infections during their latent infections, so far as is known at this time [ 17 ].…”

Ischemia–Reperfusion Injury and Immunosuppressants Promote Polyomavirus Replication Through Common Molecular Mechanisms

“…Actually, the limited genome size and coding capacity of polyomavirus determine that it has to utilize multiple host cell replication elements to complete the viral replication cycle (19,20). BKPyV may "hijack" the mechanisms of kidney repair and regeneration to promote its own replication (21). We speculated that renal IRI initiated cell regeneration, thereby creating a more favorable microenvironment for polyomavirus replication (22).…”

Smuggle tau through a secret(ory) pathway

“…Trypanosoma cruzi) could gain access to the host cytosol by rapidly degrading the host membranes within which they are internalized [4,5]. Some bacterial toxins, plant lectins, and polyomaviruses travel via retrograde transport to the endoplasmic reticulum (ER), where they exploit ER-associated degradation (ERAD) pathway to cross into the cytosol [6][7][8][9]. Escaping the cell from the cytosol is also tightly controlled.…”